Kiyotaka Kaku

Hypertrophic nonobstructive cardiomyopathy: A precise assessment of hemodynamic characteristics and clinical implications

A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.

Prevalence of the coexistence of left ventricular false tendons and premature ventricular complexes in apparently healthy subjects: a prospective study in the general population.

The prevalence of left ventricular false tendons, premature ventricular complexes and their coexistence was evaluated prospectively in 187 healthy company workers aged 21 to 50 (mean 36) years. False tendons were demonstrated echocardiographically in 133 (71%). Eight subjects were withdrawn from the study because of silent mitral valve prolapse. In these 179 healthy subjects, false tendons were detected in 127 (71%) and premature ventricular complexes in 48 (27%). Their coexistence was observed in 40, which showed a significant correlation (p less than 0.05) of false tendons and premature ventricular complexes. In seven of the eight subjects without false tendons, premature ventricular complexes were uniform and infrequent (mean 3 beats/24 h). In the 40 subjects with false tendons, premature ventricular complexes were uniform in 29, multiform in 6 and repetitive in 5, and the mean frequency was 96 beats/24 h. Correlation of premature ventricular complexes with the type of false tendons showed that premature ventricular complexes were significantly associated with thick (greater than or equal to 2 mm) and longitudinal tendons (p less than 0.005). Although it is not certain that left ventricular false tendons are arrhythmogenic, the prevalence of the coexistence of left ventricular false tendons and premature ventricular complexes in the general population, and the special relation between the frequency and the form of premature ventricular complexes and the type of false tendons, suggests that false tendons may play an etiologic role in the genesis of premature ventricular complexes in apparently healthy subjects.

Mechanisms of compensation and decompensation in dilated cardiomyopathy

Left ventricular (LV) function was evaluated in 32 patients with dilated cardiomyopathy (DC) who underwent cardiac catheterization during the past 6 years (group 4), and the results were compared with the data of 30 normal subjects (group 1). The patients were divided into mildly (group 2, 12 patients) and severely symptomatic subgroups (group 3, 20 patients). DC was characterized by dilated and poorly contracting left ventricle with increased muscle mass, reduced cardiac output and elevated systemic vascular resistance. LV volume was larger, ejection fraction was lower, and end-diastolic and end-systolic stresses were higher in group 3 than in groups 1 and 2. No significant differences were seen in LV muscle mass and wall thickness between groups 2 and 3. A significant inverse correlation was seen between ejection fraction and end-systolic stress in patients with DC (Y = -0.05x + 48.7, r = 0.57, p less than 0.01). The slope of the correlation line between end-systolic stress and volume in DC (Y = 1.20x + 135, r = 0.52, p less than 0.02) was less steep than that of normal subjects (Y = 3.68x + 40, r = 0.64, p less than 0.001). These observations indicate that the primary problem of DC is depressed contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Nifedipine on Cardiovascular System, with Special Reference to Coronary Circulation

Hypertrophic cardiomyopathy (HCM) has been believed to be a disease of diastole, while systolic functions are normal or supernormal (Goodwin 1970; Wynne and Braunwald 1984). As such, the disease involves impaired left ventricular (LV) relaxation and reduced compliance. The traditional concept of supernormal systolic function has been questioned recently by some investigators (Hirota et al. 1982; Pouleur et al. 1983), and the development of congestive heart failure associated with dilated and poorly contracting left ventricle has received substantial attention (Fujiwara et al. 1984; Yutani et al. 1985; Fighali et al. 1987). Inadequate blood supply to the myocardium due either to elevated LV diastolic pressure or to the presence of small-vessel disease may be responsible for the clinical deterioration (Fujiwara et al. 1984; Maron et al. 1986).